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156
should be considered in any patient who presents with one or more of the fol-
lowing: prolonged shock (acidosis, hypothermia, hemorrhage, coagulopathy),
visceral ischemia/perforation, traumatic injury, sepsis, massive fluid resuscita-
tion (>5 L in 24 h), ruptured abdominal aneurysm, retroperitoneal hemorrhage,
abdominal neoplasm, liver dysfunction/ascites, pancreatitis, burns, or ileus/
gastroparesis.
Finally, the severity of IAP is less important than the duration of IAH. Prolonged
elevations in IAP result in organ dysfunction and failure that can have a significant
impact upon patient morbidity and mortality [7]. Every effort should be made to
reduce the period of time that a critically ill patient’s IAP exceeds 15 mmHg, the
threshold at which most IAP-induced organ dysfunction occurs. The duration of
IAH and/or development of ACS correlate significantly with increased ICU and
hospital length of stay, patient care costs, duration of mechanical ventilation, and
patient mortality [8, 9].
13.3 Intensive Care Unit Management
While surgical decompression is widely and erroneously considered the only treat-
ment for IAH/ACS, nonoperative medical management plays a vital role in both the
prevention and treatment of IAP-induced organ dysfunction and failure [10]
(Fig. 13.1). Appropriate management of IAH/ACS is based upon four general
principles:
1. Serial monitoring of IAP
2. Optimization of systemic perfusion and end-organ function
3. Institution of organ-specific therapies to reduce IAP and avoid the detrimental
end-organ consequences of IAH/ACS
4. Prompt surgical decompression for refractory IAH/ACS
13.3.1 Sedation and Analgesia
Pain, agitation, ventilator dyssynchrony, and use of accessory muscles during work
of breathing may all lead to increased thoracoabdominal muscle tone and decreased
abdominal wall compliance, resulting in elevated IAP. Appropriate patient sedation
and analgesia can reduce muscle tone and potentially decrease IAP to less detrimen-
tal levels. In addition to ensuring patient comfort, therefore, adequate sedation and
analgesia also serve a useful therapeutic role in the patient with IAH. The goal
should be to reduce IAP to less detrimental levels and raise APP above 60 mmHg to
ensure adequate systemic perfusion. In patients with significant elevations in IAP,
sedation and analgesia to a level of general anesthesia may be necessary to over-
come increased abdominal wall tone.
M.L. Cheatham and K. Safcsak
157
13.3.2 Nasogastric/Colonic Decompression, Prokinetic Motility
Agents
Gastrointestinal ileus is common among patients who have had abdominal sur-
gery, peritonitis, major trauma, significant fluid resuscitation, or electrolyte abnor-
malities, many of which are independent risk factors for IAH/ACS. Excessive air
and fluid within the hollow viscera, as a space-occupying structure, can raise IAP
and lead to organ dysfunction and failure. Nasogastric and/or rectal drainage,
enemas, and even endoscopic decompression are relatively noninvasive methods
for reducing IAP and treating mild to moderate IAH in patients with visceral dis-
tention. Administration of prokinetic motility agents such as erythromycin,
IAH / ACS Non-Operative Management Algorithm
IAP/ APP is measured every 4-6 hours in the patient at risk for IAH / ACS. The following interventions should be applied in a stepwise fashion to maintain
an IAP
£ 15 mmHg and APP ≥ 60 mmHg. If there is no response to a particular intervention, therapy should be escalated to the next step in the algorithm.
IAH / ACS refractory to these interventions should result in abdominal decompression where appropriate.
Patient has IAP ≥ 12 mmHg
Begin medical management to reduce IAP
Evacuate
intraluminal
contents
Evacuate intra-
abdominal space
occupying lesions
Insert nasogastric
and/or rectal tube
Improve abdominal
wall compliance
Optimize fluid
adminstration
Ensure adequate
sedation &
analgesia
Optimize systemic/
regional perfusion
Avoid excessive
fluid resuscitation
Goal-directed fluid
resuscitation
Aim for zero to
negative fluid
balance by day 3
Remove
constrictive
dressings,
abdominal eschars
Maintain
App
≥
60 mmHg
Resuscitate using
hypertonic fluids,
colloids
Abdominal
ultrasound to
identify drainable
lesions
Initiate gastro-/
colo-prokinetic
agents
IAP
12 mmHg
15 mmHg
Progression of IAH
20 mmHg
ACS
25 mmHg
Concentrated
enteral nutrition
Avoid prone
position, head of
bed
> 20 degrees
Administer enemas
Abdominal
computed
tomography to
identify lesions
Consider reverse
Trendelenberg
position
Hemodynamic
monitoring to guide
resuscitation
Consider
colonoscopic
decompression
Percutaneous
catheter drainage
of fluid
Fluid removal
through judicious
diuresis once
stable
Vasoactive
medications to
keep APP
≥ 60
mmHg
Discontinue enteral
nutrition if visceral
malperfusion is
present
Consider surgical
evacuation of
lesions
Consider
neuromuscular
blockade
Consider
hemodialysis /
Ultrafiltration
If IAP > 25 mmHg (and/or APP < 50 mmHg) and new organ dysfunction / failure is present, patient’s IAH / ACS is
refractory to medical management. Strongly consider surgical abdominal decompression.
Fig. 13.1 Intensive care unit management of IAH/ACS. IAP intra-abdominal pressure, APP
abdominal perfusion pressure, IAH intra-abdominal hypertension, ACS abdominal compartment
syndrome. Modified with permission from: Cheatham ML, World J Surg. 2009;33:1116–1122
13 Intensive Care Unit Management of the Adult Open Abdomen
158
metoclopramide, or neostigmine is also useful in evacuating intraluminal contents
and decreasing visceral volume. All patients with elevated IAP should undergo
nasogastric decompression (with colonic decompression if clinically indicated).
This simple and commonly overlooked maneuver can frequently reduce IAP, raise
APP, improve visceral perfusion, and decrease the need for more aggressive
interventions.
13.3.3 Patient Positioning/Avoidance of Constrictive Dressings
Appropriate patient positioning can significantly impact IAP. The classic
Fowler’s patient position with both head and feet elevated compresses the
abdominal cavity between both the rigid ribcage and pelvis, resulting in elevated
IAP. Maintaining the spine and legs in the same axis avoids this unnecessary
abdominal compression and can reduce IAP and improve APP. When head of bed
elevation is necessary to improve respiratory effort, minimize pulmonary aspira-
tion, or facilitate treatment of traumatic brain injury, use of the reverse
Trendelenburg position can accomplish all of these goals simultaneously while
avoiding abdominal compression and elevated IAP [11]. Abdominal binders and
constrictive dressings should be avoided for similar reasons as these can also
increase IAP. In burn patients, abdominal escharotomy is particularly effective in
reducing IAP and improving APP.
13.3.4 Goal-Directed Fluid Resuscitation
Hypovolemia aggravates the pathophysiologic effects of elevated IAP, while hyper-
volemia (i.e., excessive crystalloid volume resuscitation) is an independent predic-
tor for the development of ACS. The fluid status of patients at risk for IAH/ACS
should be carefully scrutinized to avoid over-resuscitation. Careful monitoring and
maintenance of urinary output at no more than 0.5 mL/kg/h is appropriate. Fluid
losses from an open abdomen, if present, must be considered for accurate patient
fluid balance assessment. High-rate maintenance fluid infusions should be avoided
as this tends to result in excessive fluid administration over time. When necessary,
frequent, small-volume as opposed to large-volume fluid boluses should be utilized
to avoid over-resuscitation. Hypertonic crystalloid and colloid-based resuscitation
have been demonstrated to reduce IAP and decrease the risk of iatrogenic,
resuscitation- induced, increases in IAP. In critically ill patients, invasive hemody-
namic monitoring using volumetric-based monitoring technologies can be very use-
ful in assessing intravascular volume status and optimizing patient resuscitation.
Traditional pressure-based parameters such as pulmonary artery occlusion pressure
and central venous pressure have been found to be inaccurate in the presence of
elevated intra-abdominal and intrathoracic pressure and can lead to erroneous clini-
cal decisions regarding fluid status.
M.L. Cheatham and K. Safcsak
159
13.3.5 Diuretics and Continuous Venovenous Hemofiltration/
Ultrafiltration
Early intermittent hemodialysis or continuous hemofiltration/ultrafiltration may be
more appropriate than continuing to volume load the patient and increase the likeli-
hood of secondary ACS with its attendant morbidity and mortality. Fluid output
from an open abdomen actually serves as a form of peritoneal dialysis and can help
avoid the development of acute renal failure in the anuric/oliguric patient. Diuretic
therapy, in combination with colloid, may be considered to mobilize third-space
edema and reduce IAP once the patient is hemodynamically stable. These therapies
must be utilized with caution, however, as they tend to decrease APP and may
worsen the patient’s systemic perfusion if not carefully monitored.
13.3.6 Neuromuscular Blockade (NMB)
Diminished abdominal wall compliance due to pain, tight abdominal closures, and
third-space fluid can increase IAP to potentially detrimental levels. NMB has been
reported to be an effective method for reducing IAP in early IAH. A brief trial of
NMB for 24–48 h can be useful, in conjunction with other interventions, to reduce
IAP and allow resolution of the patient’s IAH, thus avoiding the need for decom-
pressive laparotomy. NMB is not efficacious in the presence of advanced IAH or
ACS, where delays in decompression will only serve to worsen the patient’s end-
organ failure. The potential benefits of NMB therapy must be balanced against the
risks of prolonged paralysis.
13.3.7 Mechanical Ventilation
As described in Table 13.1, elevated IAP causes cephalad deviation of the dia-
phragm, resulting in increased airway pressures and compression of the pulmonary
parenchyma. As a result, such patients are at risk of acute respiratory failure and the
need for prolonged mechanical ventilatory support. The majority of such patients
are appropriately managed using traditional volume-based modes of ventilation.
Patients are optimally ventilated using 6–8 mL/kg ideal body weight (not actual
body weight). Pressure-limited modes of ventilation are useful in patients with sig-
nificant elevations in peak and plateau airway pressures, recognizing that IAP raises
baseline intrathoracic pressure necessitating reevaluation of the therapeutic goals
typically used in patients without IAH. Positive end-expiratory pressure (PEEP) is
commonly necessary to maintain alveolar volumes and combat cephalad elevation
of the diaphragm due to IAP. At the moment of abdominal decompression, however,
the physician or respiratory therapist must be prepared to immediately reduce the
level of PEEP administered as the now unopposed excursion of the diaphragm cau-
dally can result in barotrauma to the lungs. A general rule of thumb is to reduce the
13 Intensive Care Unit Management of the Adult Open Abdomen
160
pre-decompression level of PEEP by 50% and then titrate the patient’s PEEP based
upon their subsequent oxygenation.
Patients who require abdominal decompression and maintenance of a temporary
open abdomen commonly require mechanical ventilation postoperatively.
Traditionally, such patients have been left intubated throughout the duration of their
open abdomen. Recent evidence, however, demonstrates that such patients can be
successfully extubated prior to definitive abdominal closure (Sujka et al., unpub-
lished data). This significantly reduces the total duration of mechanical ventilation,
decreases the risk for ventilator-associated pneumonia and need for tracheostomy,
and reduces both ICU and hospital length of stay. Predictors of successful extuba-
tion include higher Glasgow Coma Scores and lower Injury Severity Scores (espe-
cially the Chest Abbreviated Injury Score component) suggesting that patients who
are more alert, able to participate in post-extubation pulmonary rehabilitation, and
less severely injured are good candidates for early extubation despite an open
abdomen.
13.3.8 Nutritional Support
Appropriate and timely nutritional support is crucial to the successful resuscitation
and management of any critically ill patient. Early enteral nutrition, once the
patient’s acute shock state has been corrected and adequate visceral perfusion is
present, helps to prevent the development of ileus and bacterial translocation and
improves wound healing. Parenteral nutrition, due to its infectious complications
and increased cost, should be reserved for those patients who develop a high- volume
enterocutaneous fistula or intestinal malabsorption. Patients with mild to moderate
IAH can be successfully fed enterally, even with an open abdomen. In fact, enteral
nutrition helps to reduce intestinal edema and can speed the process of definitive
abdominal closure. Enteral nutrition should be held in the presence of low APP due
to concern for worsening visceral ischemia. Nutritional support should begin with a
caloric goal of 30 kcal/kg/day and protein goal of 1.5 gm/kg/day. High-protein,
high-calorie formulas allow nutritional requirements to be met with decreased total
feeding volumes and less potential for worsening the patient’s IAP. Our preference
is to use 2 kcal/mL formulas as the total daily feeding volume is generally well
tolerated even in the presence of moderate IAH. It is important to account for addi-
tional protein losses from the open abdomen, if present, by replacing each liter of
peritoneal fluid lost with 12.5 gm of protein (2 gm of nitrogen) [12].
13.3.9 Vasoactive Medications
In order to maintain an adequate APP in the presence of elevated IAP, the patient’s
blood pressure (and therefore MAP) may need to be supported using vasoactive med-
ications such as norepinephrine. This therapy should be implemented only after
ensuring adequate intravascular volume administration to avoid causing unnecessary
M.L. Cheatham and K. Safcsak
161
vasoconstriction and worsening visceral ischemia. The use of vasoactive medications
to augment APP in the euvolemic patient, however, helps to avoid excessive volume
resuscitation and is more easily titrated than fluid administration.
13.3.10 Percutaneous Decompression
Percutaneous catheter drainage of free intra-abdominal fluid, air, abscess, or blood is an
effective technique for reducing IAP and potentially correcting IAH-induced organ dys-
function. Performed under ultrasound or computed tomography guidance, percutaneous
decompression can significantly reduce IAP and decrease the need for and morbidity of
surgical decompression. This minimally invasive approach to IAH/ACS management is
most effective in patients with secondary ACS due to excessive resuscitation, burns,
acute pancreatitis, or ascites [13]. Patients with IAH/ACS refractory to percutaneous
catheter decompression should undergo urgent abdominal decompression.
13.3.11 Abdominal Decompression
Surgical decompression of the abdomen has long been the standard treatment for
IAH/ACS [5, 14, 15]. It can be lifesaving when a patient’s organ dysfunction and/or
failure are refractory to medical treatment. Delayed abdominal decompression and
disregard of high IAP levels are associated with significant increases in patient mor-
tality. Prophylactic decompression and creation of a temporary abdominal closure
in surgical patients at risk for elevated IAP significantly reduce the subsequent
development of IAH/ACS and improve survival. Emergent decompression may be
performed either in the operating room or at the patient’s bedside in the intensive
care unit if cardiopulmonary instability precludes safe transport. While seemingly
aggressive and disabling, patients at risk for IAH/ACS who are treated with abdom-
inal decompression demonstrate identical long-term physical and mental health
function as well as resumption of gainful employment compared to similar patients
who do not require an open abdomen [8, 9]. This potentially lifesaving technique,
therefore, should not be withheld from a patient who is demonstrating signs of ACS.
13.4 Strategy Overview
Based upon both clinical evidence and over two decades of high-volume experi-
ence, we share our management algorithm for the intensive care unit patient with
elevated IAP. First, serial IAP measurements are performed liberally due to the
significant incidence of IAH in the high-risk patient and its significant associated
morbidity and mortality. Second, immediate abdominal decompression is per-
formed in any patient who is found to have evidence of ACS. This procedure is
appropriate given that early decompression significantly improves survival and the
patient’s open abdomen can generally be closed within the first week without
13 Intensive Care Unit Management of the Adult Open Abdomen
162
significant long-term residual physical or mental health deficits. Third, in the patient
with IAH, but no ACS, APP is maintained above 60 mmHg through the implemen-
tation of the nonoperative interventions described above. We do not excessively
resuscitate patients simply to maintain an APP above 60 mmHg if their organ perfu-
sion and function are adequate with an APP between 50 and 60 mmHg. Fourth,
inability to maintain a minimum APP of 50 mmHg is an indication for decompres-
sive laparotomy and maintenance of an open abdomen, using a temporary abdomi-
nal closure until the patient’s clinical status improves. Fifth, post-decompression
monitoring of IAP continues as, contrary to popular belief, IAH and ACS can recur
and visceral perfusion can still be inadequate despite an open abdomen. Inability to
maintain an appropriate APP is an indication to decompress the abdomen further
through either a larger laparotomy or placement of a more compliant temporary
abdominal closure. Sixth, attempts to close the patient’s abdomen after decompres-
sion are guided by the patient’s IAP and APP. While same-admission primary fas-
cial closure should always be the goal following decompressive laparotomy,
persistent elevations in IAP with marginal APP calculations should lead to a surgi-
cal decision for either split-thickness skin grafting of the exposed viscera or skin-
only closure, as opposed to attempts to tightly close the abdominal wall. Active
communication between intensivist and surgeon is vital in the successful manage-
ment of these patients. Inappropriate fascial closure commonly results in recurrent
ACS, decreased visceral perfusion, and a high mortality rate.
Conclusion
The ICU patient with elevated IAP represents one of the most complex patients
that an intensivist can care for. Such patients are at high risk for multisystem
organ dysfunction and failure, especially if the patient’s elevated IAP is not rec-
ognized and appropriately addressed in a timely fashion. The management strat-
egy outlined above has been continuously developed in our ICUs during the care
of thousands of patients with elevated IAP over the past two decades. It has been
demonstrated to reduce the morbidity of IAH/ACS and significantly improve
patient survival. Adoption of such a multimodality, evidence-based management
strategy can be expected to achieve similar results in any ICU.
Take-Home Messages
1. IAP should be measured in all critically ill patients with evidence of organ
dysfunction and/or failure.
2. Implemented early, multimodality nonoperative management can reduce
IAP and prevent progression of IAH to ACS.
3. Immediate surgical decompression should be performed in the presence of
ACS or when adequate end-organ perfusion and function cannot be
maintained.
4. Patient survival from IAH/ACS is significantly improved by adopting a
comprehensive ICU management strategy.
M.L. Cheatham and K. Safcsak
163
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parameter in the assessment of intra-abdominal hypertension. J Trauma. 2000;49:621–7.
7. Kyoung K, Hong S. The duration of intra-abdominal hypertension strongly predicts outcomes
for the critically ill surgical patient: a prospective observational study. World J Emerg Surg.
2015;10:22.
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and functional consequences of abdominal decompression. J Trauma. 2004;56:237–42.
9. Cheatham ML, Safcsak K, Sugrue M. Long-term implications of intra-abdominal hyper-
tension and abdominal compartment syndrome: physical, mental, and financial. Am Surg.
2011;77(Suppl 1):S78–82.
10. Kirkpatrick AW, Roberts DJ, De Waele J, Jaeschke R, Malbrain ML, et al. Intra-abdominal
hypertension and the abdominal compartment syndrome: updated consensus definitions and
clinical practice guidelines from the World Society of the Abdominal Compartment Syndrome.
Intensive Care Med. 2013;39:1190–206.
11. De Keulenaer BL, Cheatham ML, De Waele JJ, Kimball EJ, Powell B, Davis WA, Jenkins
IR. Intra-abdominal pressure measurements in lateral decubitus versus supine position. Acta
Clin Belg. 2009;64:210–5.
12. Cheatham ML, Safcsak K, Brzezinski SJ, Lube MW. Nitrogen balance, protein loss, and the
open abdomen. Crit Care Med. 2007;35(1):127–31.
13. Cheatham ML, Safcsak K. Percutaneous catheter decompression in the treatment of elevated
intra-abdominal pressure. Chest. 2011;140:1428–35.
14. Coccolini F, Biffl W, Catena F, Ceresoli M, Chiara O, et al. The open abdomen, indications,
management, and definitive closure. World J Emerg Surg. 2015;10:32.
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13 Intensive Care Unit Management of the Adult Open Abdomen
165
© Springer International Publishing AG, part of Springer Nature 2018
F. Coccolini et al. (eds.), Open Abdomen, Hot Topics in Acute Care Surgery
and Trauma, https://doi.org/10.1007/978-3-319-48072-5_14
T. Kaussen
Department of Pediatric Cardiology and Intensive Care Medicine, Hannover Medical School,
Carl-Neuberg-Street 1, 30625 Hannover, Germany
e-mail: torsten.kaussen@gmx.de
14
Management of the Open Abdomen
in PICU
Torsten Kaussen
14.1 Historical Development and Background
From a historical perspective, the open abdomen (OA; syn. abdomen apertum, lap-
arostoma, temporary abdominal closure [TAC]) is a form of treatment in pediatric
surgery that emerged with the development of methods to temporarily expand as
well as reconstruct the abdominal wall within the framework of operative care for
inborn abdominal wall defects [1–3]. It is in the context of abdominal wall approxi-
mation and adaptation that gastroschisis and omphalocele are still considered proto-
types for diseases often leading to a predisposition for intra-abdominal hypertension
(IAH) and abdominal compartment syndrome (ACS) [4–6].
One speaks of an IAH in children starting at an intra-abdominal pressure (IAP)
of 10 mmHg [7]. According to Kron et al. [8], the pediatric gold standard for IAP
quantification is the modified measurement of bladder pressure. Further methods
are used—albeit much less often—in everyday clinical practice [9–14]. The most
notable technique involves continual indirect measurement of IAP via the stomach
(IAP-monitor of Fa. Spiegelberg
®
, Hamburg). Following increases in IAP of only
6–8 mmHg in premature infants and newborns, cardiorespiratory limitations have
been observed and described [15, 16]; however, the most recent data does not allow
for a definition of limits adapted to percentiles. Depending on the level of IAP val-
ues, four non-percentile-adjusted IAH severity grades apply (see Table 14.1) [17].
Starting at Grade II, there is an increased transition into a complete ACS defined by
the additional occurrence or aggravation of pending organ dysfunction (OD; OD
criteria, Table 14.2) [18].
166
Table 14.1 Child-oriented adapted WSACS consensus definitions [7, 17]
IAP Pressure within the abdominal cavity (mmHg, measured at end expiration)
Normal IAP 7 ± 3 mmHg in critically ill children
APP
RFG
IAH
=MAP−IAP (abdominal perfusion pressure = mean arterial pressure minus
IAP)
=MAP−2 × IAP (renal filtration gradient)
Sustained or repeated pathological elevation in IAP ≥ 10 mmHg
– Grade I
– Grade II
– Grade III
– Grade IV
IAP 10–12 mmHg
IAP 13–15 mmHg
IAP 16–18 mmHg
IAP > 18 mmHg
ACS Sustained IAP ≥ 10 mmHg associated with new organ dysfunction/failure
Primary ACS Condition associated with injury or disease in the abdominopelvic region
Secondary ACS Condition that does not originate from the abdominopelvic region
Recurrent ACS Condition in which ACS redevelops after previous surgical or medical
treatment of primary or secondary ACS
Table 14.2 Diagnostic criteria for organ dysfunction
Cardiovascular Despite intravenous application of ≥40 mL/kg isotonic volume in 60 min
persisting
• Hypotension with BP <5th percentile for age or systolic BP < 2 SD
below normal for age
• Vasoactive drug therapy to keep BP in normal range
• Two of the following
– Arterial lactate >2 times upper limit of normal
– Prolonged capillary refill >5 s
– Oliguria, urine output <0.5 mL/kg/h
– Metabolic acidosis (base deficit >5 mmol/L)
– Core to peripheral body temperature difference >3°C
Hematologic • Thrombocyte count <80,000/mm
3
or decline of 50% in thrombocyte
count from the highest value recorded over the past 3 days
• INR > 2
Hepatic • Total bilirubin ≥4 mg/dL (not applicable for newborn)
• ALT two times upper limit of normal age
Neurologic • Glasgow Coma Scale (GCS) ≤11
• Acute change in mental status with decrease in GCS ≥3 points from
abnormal baseline
Renal Serum creatinine ≥2 times upper limit of normal for age
Twofold rise in baseline serum creatinine
Respiratory • Oxygenation index <300 in the absence of cyanotic heart disease or
preexisting lung disease
• PaCO
2
> 65 mmHg or increase of >20 mmHg over baseline
• Proven need or FiO
2
> 0.5 in order to maintain saturation ≥92%
• Need for mechanical ventilation (invasive or noninvasive)
Cardiovascular, hematologic, hepatic, neurologic, renal, and respiratory dysfunction according to
the international pediatric sepsis consensus conference [18]
BP blood pressure, GCS Glasgow Coma Scale, ALT alanine aminotransferase
T. Kaussen